ライフサイエンスコーパス: 6-hydroxydopamine

1 to a subsequent neurotoxic trigger (low-dose 6-hydroxydopamine).

2 rkinsonian rodent model induced by the toxin 6-hydroxydopamine.

3 ease based on neuronal PC12 cells exposed to 6-hydroxydopamine.

4 from death induced by hydrogen peroxide and 6-hydroxydopamine.

5 ons that antioxidants confer protection from 6-hydroxydopamine.

6 eeks after unilateral lesions of the SN with 6-hydroxydopamine.

7 eived unilateral intrastriatal injections of 6-hydroxydopamine.

8 lesioned as neonates (neonate lesioned) with 6-hydroxydopamine.

9 stress is compromised were more sensitive to 6-hydroxydopamine.

10 expression on neuronal PC12 cells exposed to 6-hydroxydopamine.

11 e neurons when administered 6 h prior to the 6-hydroxydopamine.

12 d 6 h later with an intranigral injection of 6-hydroxydopamine.

13 endoplasmic reticulum (ER) stress induced by 6-hydroxydopamine.

14 by intrastriatal injection of the neurotoxin 6-hydroxydopamine.

15 y following administration of the neurotoxin 6-hydroxydopamine.

16 when worms were exposed to the DA neurotoxin 6-hydroxydopamine.

17 triatal denervation in animals injected with 6-hydroxydopamine.

18 ceptibility of retinal dopaminergic cells to 6-hydroxydopamine.

19 ateral intrastriatal injections of the toxin 6-hydroxydopamine.

20 6-hydroxydopamine, 1-methyl-4-phenyl-pyridinium (MPP+),

21 ts treated with splanchnic ganglionectomy or 6-hydroxydopamine (6-OH-dopamine).

22 ative effects of the dopaminergic neurotoxin 6-hydroxydopamine (6-OHDA) (unilateral intrastriatal inj

23 lateral lesion in substantia nigra (SN) with 6-hydroxydopamine (6-OHDA) affected differently the exci

24 ted by the Parkinsonism-inducing neurotoxins 6-hydroxydopamine (6-OHDA) and 1-methyl-4-phenylpyridini

25 naptic dopamine transporter (DAT), including 6-hydroxydopamine (6-OHDA) and 1-methyl-4-phenylpyridini

26 reated with the dopaminergic neuronal toxins 6-hydroxydopamine (6-OHDA) and 1-methyl-4-phenylpyridini

27 PD in vitro, including an oxidative stressor 6-hydroxydopamine (6-OHDA) and a proteasome inhibitor MG

28 has been investigated as a treatment in the 6-hydroxydopamine (6-OHDA) animal model of PD.

29 n's disease described in the pharmacological 6-hydroxydopamine (6-OHDA) animal models of Parkinson's

30 Rats lesioned with 6-hydroxydopamine (6-OHDA) as neonates exhibit behaviora

31 exacerbates vulnerability to the neurotoxin 6-hydroxydopamine (6-OHDA) both in vitro and in vivo.

32 activated at the transcriptional level in a 6-hydroxydopamine (6-OHDA) cellular model of PD.

33 neurotrophic factor GDNF in the unilaterally 6-hydroxydopamine (6-OHDA) denervated substantia nigra (

34 We previously found that 6-hydroxydopamine (6-OHDA) elicits sustained extracellul

35 The neurotoxin, 6-hydroxydopamine (6-OHDA) has been implicated in the ne

36 The neurotoxin 6-hydroxydopamine (6-OHDA) has been used extensively in

37 eroxide (TBHP) and of the dopaminergic toxin 6-hydroxydopamine (6-OHDA) in PC12 cells.

38 by 1-methyl-4-phenylpyridinium (MPP(+)) and 6-hydroxydopamine (6-OHDA) in primary DAergic neuron cul

39 we induce DAergic neuronal loss by injecting 6-hydroxydopamine (6-OHDA) in the dorsal GL or in the ri

40 sion of saline vehicle containing or lacking 6-hydroxydopamine (6-OHDA) in the ipsilateral medial for

41 tudy, we demonstrate that rats lesioned with 6-hydroxydopamine (6-OHDA) in the medial forebrain bundl

42 ministration of the catecholamine neurotoxin 6-hydroxydopamine (6-OHDA) induced a selective depletion

43 o investigate the in vivo effects of BMP7 on 6-hydroxydopamine (6-OHDA) induced lesioning of midbrain

44 Six weeks after 6-hydroxydopamine (6-OHDA) infusion into the medial fore

45 ssive degeneration induced by the neurotoxin 6-hydroxydopamine (6-OHDA) injected into the striatum.

46 immunoreactive microglial profiles following 6-hydroxydopamine (6-OHDA) injection into ipsilateral st

47 Animals previously given 6-hydroxydopamine (6-OHDA) injections into the ascending

48 One week following two bilateral 6-hydroxydopamine (6-OHDA) injections into the mPFC, ani

49 aporin (SAP) into the basal forebrain and/or 6-hydroxydopamine (6-OHDA) into the caudate nucleus, res

50 Five rats received unilateral injection of 6-hydroxydopamine (6-OHDA) into the medial forebrain bun

51 D was induced with a unilateral injection of 6-hydroxydopamine (6-OHDA) into the medial forebrain bun

52 triatal lesioning was performed by injecting 6-hydroxydopamine (6-OHDA) into the substantia nigra par

53 6-Hydroxydopamine (6-OHDA) is an oxidative neurotoxin us

54 While 6-hydroxydopamine (6-OHDA) is often used in animal model

55 The dopamine analogue 6-hydroxydopamine (6-OHDA) is selectively toxic to catec

56 6-Hydroxydopamine (6-OHDA) is widely used to selectively

57 igrostriatal dopamine system by injection of 6-hydroxydopamine (6-OHDA) lead to abnormal neuronal act

58 havioral protection against an intrastriatal 6-hydroxydopamine (6-OHDA) lesion in the common marmoset

59 s of reserpine-induced akinesia, and the rat 6-hydroxydopamine (6-OHDA) lesion model of drug-induced

60 use model of reserpine-induced akinesia, rat 6-hydroxydopamine (6-OHDA) lesion model of drug-induced

61 ffects of a partial unilateral intrastriatal 6-hydroxydopamine (6-OHDA) lesion model of PD on the num

62 We exploited the unilateral 6-hydroxydopamine (6-OHDA) lesion model to assess the ef

63 motor deficits in a unilateral nigrostriatal 6-hydroxydopamine (6-OHDA) lesion model using optogeneti

64 neurons in the progressive Sauer and Oertel 6-hydroxydopamine (6-OHDA) lesion model, rats received p

65 ridol-induced catalepsy in mouse and the rat 6-hydroxydopamine (6-OHDA) lesion model.

66 44BNF(1)) hybrid rats following a unilateral 6-hydroxydopamine (6-OHDA) lesion of the nigrostriatal p

67 and amphetamine-induced rotations caused by 6-hydroxydopamine (6-OHDA) lesion.

68 n-1 (OP-1), on the progression of a striatal 6-hydroxydopamine (6-OHDA) lesion.

69 Administration of dopamine agonists to 6-hydroxydopamine (6-OHDA) lesioned rats enhances the ro

70 es from the striatum of intact or unilateral 6-hydroxydopamine (6-OHDA) lesioned rats of increasing a

71 n dopamine denervated striatum of unilateral 6-hydroxydopamine (6-OHDA) lesioned rats.

72 One model was 6-hydroxydopamine (6-OHDA) lesioning and the other was d

73 Rats were given unilateral 6-hydroxydopamine (6-OHDA) lesions and subsequently rece

74 N) on motor impairment induced by unilateral 6-hydroxydopamine (6-OHDA) lesions in the medial forebra

75 6-Hydroxydopamine (6-OHDA) lesions of brain noradrenergi

76 Rats with 6-hydroxydopamine (6-OHDA) lesions of the nigrostriatal

77 To this end, we tested animals with 6-hydroxydopamine (6-OHDA) lesions of the PL and IL mPFC

78 ced turning behavior in rats with unilateral 6-hydroxydopamine (6-OHDA) lesions of the SN.

79 phine administration in rats with unilateral 6-hydroxydopamine (6-OHDA) lesions of the substantia nig

80 Nigral 6-hydroxydopamine (6-OHDA) lesions or repeated D2-class

81 Partial 6-hydroxydopamine (6-OHDA) lesions were conducted in the

82 s not altered by decortication or unilateral 6-hydroxydopamine (6-OHDA) lesions.

83 striatal slices from rodents with unilateral 6-hydroxydopamine (6-OHDA) lesions.

84 tions were assessed in a mouse intrastriatal 6-hydroxydopamine (6-OHDA) model of hemiparkinsonism.

85 ioning (TPC) was found to be protective in a 6-hydroxydopamine (6-OHDA) model of the disease.

86 iatal catecholamine levels in the unilateral 6-hydroxydopamine (6-OHDA) mouse model of dopaminergic c

87 n the early neurochemical events involved in 6-hydroxydopamine (6-OHDA) neurotoxicity and the putativ

88 ive, central noradrenergic dennervation with 6-hydroxydopamine (6-OHDA) on the expression of type 4 p

89 ted with bilateral microinjections of either 6-hydroxydopamine (6-OHDA) or its vehicle into the NAcc

90 mine and metabolite levels in mice receiving 6-hydroxydopamine (6-OHDA) or rotenone to simulate PD.

91 s, into the area of neurodegeneration in the 6-hydroxydopamine (6-OHDA) PD model.

92 clic antidepressant was neuroprotective in a 6-hydroxydopamine (6-OHDA) rat model of parkinsonism.

93 of amelioration of motor asymmetry in adult, 6-hydroxydopamine (6-OHDA) rats.

94 cardiomyocyte growth was investigated using 6-hydroxydopamine (6-OHDA) to abolish early sympathetic

95 ortex (mPFC) were unilaterally lesioned with 6-hydroxydopamine (6-OHDA) to examine how dopamine (DA)

96 t study, we used the dopaminergic (DA) toxin 6-hydroxydopamine (6-OHDA) to model PD and explore the p

97 2,3,6-tetrahydropyridine toxicity in mice or 6-hydroxydopamine (6-OHDA) toxicity in rats.

98 y protects midbrain dopamine neurons against 6-hydroxydopamine (6-OHDA) toxicity.

99 r (GDNF) protects dopamine (DA) neurons from 6-hydroxydopamine (6-OHDA) toxicity.

100 translocation were increased in response to 6-hydroxydopamine (6-OHDA) treatment.

101 The data indicate that the different 6-hydroxydopamine (6-OHDA) vulnerabilities of ventral me

102 e current studies, unilateral, intrastriatal 6-hydroxydopamine (6-OHDA) was used to investigate how d

103 h D3T for 24 h and then exposed to dopamine, 6-hydroxydopamine (6-OHDA), 4-hydroxy-2-nonenal (HNE), o

104 Neurotoxin lesions with 6-hydroxydopamine (6-OHDA), 5,7-dihydroxytryptamine (5,7

105 rn of neurodegeneration after treatment with 6-hydroxydopamine (6-OHDA), a neurotoxin commonly used t

106 tum 4 weeks after intrastriatal injection of 6-hydroxydopamine (6-OHDA), a neurotoxin selective for c

107 6-Hydroxydopamine (6-OHDA), a PD mimetic, is widely used

108 However, others have shown that injection of 6-hydroxydopamine (6-OHDA), a toxin devoid of saporin, a

109 tion of catechols, such as dopamine (DA) and 6-hydroxydopamine (6-OHDA), and resulting in oxidative s

110 phic factor (GDNF), when administered before 6-hydroxydopamine (6-OHDA), has been shown to prevent th

111 an SH-SY5Y - after treatment with neurotoxin 6-hydroxydopamine (6-OHDA), leading to the biosynthesis

112 nd neurotoxic lesions of DA neurons by using 6-hydroxydopamine (6-OHDA), to ascertain whether N/OFQ a

113 The neurotoxin 6-hydroxydopamine (6-OHDA), which is easily oxidized to

114 The 6-hydroxydopamine (6-OHDA)-induced destruction of the ni

115 and indirect projecting systems arises after 6-hydroxydopamine (6-OHDA)-induced dopamine depletion, h

116 treadmill locomotion in rats with unilateral 6-hydroxydopamine (6-OHDA)-induced lesions of nigrostria

117 The effects of 6-hydroxydopamine (6-OHDA)-induced lesions of the dorsal

118 Severe 6-hydroxydopamine (6-OHDA)-induced neostriatal dopamine

119 mine receptors (D(2)DRs) in the unilaterally 6-hydroxydopamine (6-OHDA)-lesioned rat enhanced striata

120 ir ability to induce rotational behaviour in 6-hydroxydopamine (6-OHDA)-lesioned rats and to potentia

121 Prior studies in unilateral 6-hydroxydopamine (6-OHDA)-lesioned rats have primarily

122 orded in freely moving normal and unilateral 6-hydroxydopamine (6-OHDA)-lesioned rats using chronical

123 In unilateral 6-hydroxydopamine (6-OHDA)-lesioned rats, (+)-dinapsolin

124 We recently reported that in 6-hydroxydopamine (6-OHDA)-lesioned striatum, norepineph

125 Remarkably, after a partial 6-hydroxydopamine (6-OHDA)-mediated DA depletion ( appro

126 e-induced rotations in the hemi-Parkinsonian 6-hydroxydopamine (6-OHDA)-treated rat and 2) locomotion

127 were subsequently infused ipsilaterally with 6-hydroxydopamine (6-OHDA).

128 riatal injection of the oxidative neurotoxin 6-hydroxydopamine (6-OHDA).

129 ation induced chemically with the neurotoxin 6-hydroxydopamine (6-OHDA).

130 ors, followed by intrastriatal injections of 6-hydroxydopamine (6-OHDA).

131 city of the catecholaminergic ROS generator, 6-hydroxydopamine (6-OHDA).

132 lateral medial forebrain bundle injection of 6-hydroxydopamine (6-OHDA).

133 loying the parkinsonism-inducing neurotoxin, 6-hydroxydopamine (6-OHDA).

134 ter unilateral exposure to the DA neurotoxin 6-hydroxydopamine (6-OHDA).

135 rotein also potentiated the neurotoxicity of 6-hydroxydopamine (6-OHDA).

136 inergic pathway was unilaterally lesioned by 6-hydroxydopamine (6-OHDA).

137 amine neurons following in vivo lesions with 6-hydroxydopamine (6-OHDA).

138 d to an unilateral intrastriatal infusion of 6-hydroxydopamine (6-OHDA).

139 th resistance to oxidative stress induced by 6-hydroxydopamine (6-OHDA).

140 nuated cell death induced by the PD-mimetic, 6-hydroxydopamine (6-OHDA).

141 SNC following treatment with the neurotoxin 6-hydroxydopamine (6-OHDA); however, GFRalpha-1 expressi

142 (PRZ, an alpha-1 adrenoceptor antagonist) or 6-hydroxydopamine (6-OHDA, an agent that induces chemica

143 l ganglia of rats, lesioned as neonates with 6-hydroxydopamine (6-OHDA, intracisternally) on the thir

144 cit and cerebral oxidative stress induced by 6-hydroxydopamine (6-OHDA; 8 mug/2 muL) injected into th

145 eral intracerebroventricular injections with 6-hydroxydopamine (6-OHDA; a model of Lesch-Nyhan syndro

146 located in the SNR, which were resistant to (6-hydroxydopamine) 6-OHDA, was established by their expr

147 clinical lesions of the striatum with either 6-hydroxydopamine (6OHDA) or quinolinic acid (QA) exagge

148 or chemical sympathectomy of the spleen with 6-hydroxydopamine (6OHDA; -14d) exacerbated injury after

149 6-Hydroxydopamine administration resulted in an increase

150 In addition, Fyn-depleted mice lesioned with 6-hydroxydopamine also failed to exhibit l-DOPA-induced

151 tomy eliminated both the survival benefit of 6-hydroxydopamine and monocyte recruitment, suggesting t

152 were given a unilateral dopamine lesion with 6-hydroxydopamine and primed with a chronic regimen of l

153 ts of unilateral nigrostriatal ablation with 6-hydroxydopamine and subsequent treatment with levodopa

154 fluorescent protein) mice were lesioned with 6-hydroxydopamine and subsequently treated with L-DOPA t

155 s induced by the intra-striatal injection of 6-hydroxydopamine, and mice were treated with either sal

156 dult mice by the intra-striatal injection of 6-hydroxydopamine, and PD mice were treated with 1mg/kg

157 ncreased in the presence of ascorbic acid or 6-hydroxydopamine as pro-oxidants.

158 nt (scid) mouse that was depleted of NE with 6-hydroxydopamine before reconstitution with a clone of

159 rm of Nix, protects neuronal PC12 cells from 6-hydroxydopamine but not from nerve growth factor depri

160 how that dopamine depletion in adult rats by 6-hydroxydopamine caused a significant decrease in stria

161 vivo on the effects of L-dopa in the 6OHDA (6-hydroxydopamine) contralateral turning model.

162 6-Hydroxydopamine decreased tissue concentrations of dop

163 inistration of the noradrenergic neurotoxin, 6-hydroxydopamine, did not block the effect of IL-1beta.

164 r adult rats were unilaterally lesioned with 6-hydroxydopamine, fast-scan cyclic voltammetry at Nafio

165 nigrostriatal dopamine system ablation with 6-hydroxydopamine followed by twice-daily treatment with

166 encephalon at 3, 7, 10, 14 and 21 days after 6-hydroxydopamine had been injected into the medial fore

167 synergistic attenuation of motor deficits in 6-hydroxydopamine hemilesioned rats and 1-methyl-4-pheny

168 mg/Kg) attenuated dyskinesias expression in 6-hydroxydopamine hemilesioned rats primed with L-DOPA,

169 nimals received an injection of 25 microg of 6-hydroxydopamine hydrobromide (6-OHDA) midway between t

170 halamus were lesioned by i.c.v. injection of 6-hydroxydopamine immediately prior to the induction of

171 atal dopamine neurons against the effects of 6-hydroxydopamine in aged as well as young adult rats.

172 ctive destruction of dopamine terminals with 6-hydroxydopamine, indicating that GABA release originat

173 onal cells protects against staurosporin and 6-hydroxydopamine induced apoptosis and cell death.

174 e mitochondrial JNK plays in the etiology of 6-hydroxydopamine-induced (6-OHDA) oxidative stress, mit

175 We found that meclizine protected against 6-hydroxydopamine-induced apoptosis and cell death in bo

176 These cells are vulnerable to hypoxia- and 6-hydroxydopamine-induced cell death, respectively.

177 rat nigrostriatal dopaminergic pathway from 6-hydroxydopamine-induced damage.

178 ameliorated behavioral deficits in rats with 6-hydroxydopamine-induced hemiparkinsonism.

179 re neuronal activity in the STN of rats with 6-hydroxydopamine-induced lesions of the nigrostriatal p

180 factor (GDNF) can completely protect against 6-hydroxydopamine-induced loss of nigral dopamine neuron

181 l death, neurotoxin-induced neuronal injury, 6-hydroxydopamine-induced Parkinson's dopaminergic neuro

182 GDNF pretreatment also protected against 6-hydroxydopamine-induced reductions in striatal DOPAC l

183 ventral striatal dopaminergic terminals with 6-hydroxydopamine infusions into the nucleus accumbens d

184 Depletion of dopamine by 6-hydroxydopamine injection on postnatal day 4 did not a

185 cells into rats rendered hemiparkinsonian by 6-hydroxydopamine injection.

186 tal dopamine depletions, rats first received 6-hydroxydopamine injections into the nigrostriatal bund

187 Injections of 6-hydroxydopamine into the brainstem did not reduce the

188 tive lesion of A5 cells by microinjection of 6-hydroxydopamine into the pons showed no deficits to st

189 Injections of 6-hydroxydopamine into the vPAG, which killed 55-65% of

190 Following a unilateral 6-hydroxydopamine lesion A, A(A) and double A-A(A) knock

191 The 6-hydroxydopamine lesion affected B(max) (control, 402 +

192 otection of SN neurons following progressive 6-hydroxydopamine lesion and was associated with decreas

193 Likewise, 6-hydroxydopamine lesion did not impact GABA or glutamat

194 motor neglect after unilateral nigrostriatal 6-hydroxydopamine lesion in mice.

195 rat model of Parkinson's disease, unilateral 6-hydroxydopamine lesion in the substantia nigra, [3H]AA

196 6-Hydroxydopamine lesion led to parkinsonian motor impai

197 Using the 6-hydroxydopamine lesion model of Parkinson's disease an

198 The present study used the rat unilateral 6-hydroxydopamine lesion model of Parkinson's disease to

199 n of NMDA receptor subunits (NRs) in the rat 6-hydroxydopamine lesion model of parkinsonism.

200 ects of the GDNF product in an intrastriatal 6-hydroxydopamine lesion model.

201 ue-Dawley rats initially received unilateral 6-hydroxydopamine lesion of the medial forebrain bundle.

202 Furthermore, a unilateral 6-hydroxydopamine lesion of the mesostriatal dopamine sy

203 n of the adult rat by using a combination of 6-hydroxydopamine lesion of the substantia nigra dopamin

204 Bilateral 6-hydroxydopamine lesion reduced long-term but not short

205 otational behavior in rats with a unilateral 6-hydroxydopamine lesion was used as an index of psychom

206 Neonatal rat 6-hydroxydopamine lesion-induced hyperactivity was used

207 walking states, before and after unilateral 6-hydroxydopamine lesion.

208 accumbens and caudate-putamen, 4 weeks after 6-hydroxydopamine lesion.

209 ctances, and their responsiveness to chronic 6-hydroxydopamine lesion.

210 In addition, 6-hydroxydopamine lesioned mice showed extended survival

211 In addition, in a rat 6-hydroxydopamine lesioned model of PD, chronic levodopa

212 When transplanted into the 6-hydroxydopamine lesioned Parkinsonian rats, these cogr

213 basal ganglia were studied in the unilateral 6-hydroxydopamine lesioned rat model of PD.

214 l spiking activity in control and unilateral 6-hydroxydopamine lesioned rats performing a skilled for

215 n and ipsilateral striatal Fos expression in 6-hydroxydopamine lesioned rats.

216 d the activity of L-DOPA in the unilaterally 6-hydroxydopamine-lesioned (6-OHDA) rat, a model of Park

217 In the 6-hydroxydopamine-lesioned animal model of Parkinson's d

218 ional behavior induced by apomorphine in the 6-hydroxydopamine-lesioned animal models of Parkinson's

219 Sham- and 6-hydroxydopamine-lesioned mice were subjected to the no

220 ed transcriptome analyses in the striatum in 6-hydroxydopamine-lesioned mice.

221 When transplanted into the neostriata of 6-hydroxydopamine-lesioned parkinsonian rats, the dopami

222 Toxin-based models, such as the 6-hydroxydopamine-lesioned rat and 1-methyl-4-phenyl-1,2

223 omorphine-induced rotational behavior in the 6-hydroxydopamine-lesioned rat model of hemiparkinsonism

224 omorphine-induced rotational behavior in the 6-hydroxydopamine-lesioned rat model of hemiparkinsonism

225 In the 6-hydroxydopamine-lesioned rat model, this compound was

226 A in a rat model of Parkinson's disease (the 6-hydroxydopamine-lesioned rat), dosed at 30 mg/kg orall

227 oth potentiated the effects of L-DOPA in the 6-hydroxydopamine-lesioned rat, a model of Parkinson's d

228 e neuroblastoma (NBP2) cells into striata of 6-hydroxydopamine-lesioned rats (an animal model of PD)

229 Seven unilaterally 6-hydroxydopamine-lesioned rats (dopaminergic denervatio

230 sion were compared in the STN of control and 6-hydroxydopamine-lesioned rats and mice.

231 nificantly increased in ON L-DOPA dyskinetic 6-hydroxydopamine-lesioned rats, suggesting that increas

232 ions can release dopamine in the midbrain of 6-hydroxydopamine-lesioned rats.

233 nduced dopamine-depleted mice and in chronic 6-hydroxydopamine-lesioned rats.

234 of l-dopa-induced contralateral rotations in 6-hydroxydopamine-lesioned rats.

235 , IGF-I, and bFGF and then transplanted into 6-hydroxydopamine-lesioned rats.

236 ent inhibition of locomotor hyperactivity in 6-hydroxydopamine-lesioned rats.

237 ame-day lesion-transplant paradigm) into the 6-hydroxydopamine-lesioned striatum of rats significantl

238 porcine ventral mesencephalic tissue in the 6-hydroxydopamine-lesioned, nonimmunosuppressed rat indu

239 l KOs and caffeine-pretreated mice following 6-hydroxydopamine lesioning.

240 Analysis of LTP in animals with unilateral 6-hydroxydopamine lesions (6-OHDA) rendered dyskinetic w

241 ias were evaluated twice a week in mice with 6-hydroxydopamine lesions during long-term L-DOPA (25 mg

242 t, neurons recorded in rats with ipsilateral 6-hydroxydopamine lesions failed to show attentional sig

243 We made localized intrastriatal 6-hydroxydopamine lesions in rats and recorded within th

244 6-hydroxydopamine lesions of the A5-7 groups or ibotenic

245 the present study, we examined the effect of 6-hydroxydopamine lesions of the medial prefrontal corte

246 munocytochemistry in animals with unilateral 6-hydroxydopamine lesions of the nigrostriatal bundle.

247 Unilateral 6-hydroxydopamine lesions of the nigrostriatal system we

248 ed DAMGO-induced motor activity that follows 6-hydroxydopamine lesions of the nucleus accumbens.

249 arm use, in contrast to rats with unilateral 6-hydroxydopamine lesions of the substantia nigra.

250 al caudate-putamen were determined following 6-hydroxydopamine lesions of the ventral tegmental area

251 taneous object recognition to test rats with 6-hydroxydopamine lesions targeted at the core or medial

252 found that the acute hypertension induced by 6-hydroxydopamine lesions was immediately reversed and t

253 denervated striatum of rats with unilateral 6-hydroxydopamine lesions.

254 Here, we show that 6-hydroxydopamine-mediated ablation of the mouse periphe

255 Using a model of 6-hydroxydopamine-mediated noradrenergic nerve ablation,

256 lective dopamine (DA) depleting lesions with 6-hydroxydopamine microinjection into the SN, CPu, and N

257 ydroxy-N,N-di-n-propyl-2-aminotetralin) in a 6-hydroxydopamine model of Parkinson's disease.

258 n the dopamine-depleted striatum of a rodent 6-hydroxydopamine model of Parkinson's disease.

259 e response to achieve neuroprotection in the 6-hydroxydopamine model.

260 ed a stereotaxic injection of 8 mug/2 muL of 6-hydroxydopamine (n = 6) or saline solution (n = 4) in

261 halic dopaminergic neurons protected against 6-hydroxydopamine neurotoxicity by suppressing apoptosis

262 ty in two PD animal models, reserpinized and 6-hydroxydopamine (OHDA)-induced unilateral lesioned rat

263 r77, and Nur77 knockdown were adopted in the 6-hydroxydopamine (OHDA)-lesioned PC12 cells to investig

264 ctivity in basolateral amygdala in rats with 6-hydroxydopamine or sham lesions of the ipsilateral mid

265 tures of Sprague-Dawley rats with unilateral 6-hydroxydopamine or sham lesions of the rostral accumbe

266 We microinjected 6-hydroxydopamine or vitamin C into nucleus tractus soli

267 al models of PD induced by either oxidative (6-hydroxydopamine) or mitochondrial (N-methyl-4-phenyl-1

268 were destroyed via intraocular injection of 6-hydroxydopamine over 2 successive days.

269 d quantification of DAT in rodents using the 6-hydroxydopamine Parkinson disease rat model.

270 used microPET to study unilaterally lesioned 6-hydroxydopamine rats that developed levodopa-induced a

271 t AIM severity, following induction of AIMs, 6-hydroxydopamine rats were injected with Daun02 in the

272 uction in SN of both unprimed and dyskinetic 6-hydroxydopamine rats, consistent with opposite adaptiv

273 Rats unilaterally lesioned with 6-hydroxydopamine received transplants that were incubat

274 hway produced in rats following injection of 6-hydroxydopamine result in a neurochemical profile simi

275 Intrastriatal injection of 6-hydroxydopamine results in selective toxicity to these

276 ation of the PF in the rat and determined if 6-hydroxydopamine SN lesions cause PF neuron degeneratio

277 n cerebellar granule neurons by glutamate or 6-hydroxydopamine stimulation but not potassium withdraw

278 , a group of animals received a high dose of 6-hydroxydopamine that normally would yield a severe los

279 Rats were administered 6-hydroxydopamine to induce brainstem lesions, causing a

280 urons, we have used the selective neurotoxin 6-hydroxydopamine to lesion their terminals within the s

281 s disease, including unilateral infusions of 6-hydroxydopamine to the medial forebrain bundle and per

282 Using two PD models, the traditional 6-hydroxydopamine toxic lesion and a genetic model with

283 peroxide dismutase showed no protection from 6-hydroxydopamine toxicity in either brain region.

284 racellular or nonmitochondrial mechanisms in 6-hydroxydopamine toxicity, the compartmentalization of

285 le for mitochondrially derived superoxide in 6-hydroxydopamine toxicity.

286 in the dyskinetic animals compared with the 6-hydroxydopamine-treated and control rats.

287 corded from the basal ganglia of control and 6-hydroxydopamine-treated hemi-parkinsonian rats anesthe

288 mal models of DA neuron loss and PD, such as 6-hydroxydopamine-treated mice or rats and 1-methyl-4-ph

289 lantation of these cells into the striata of 6-hydroxydopamine-treated rats at the neuronal progenito

290 to potassium removal, glutamate toxicity, or 6-hydroxydopamine treatment and found that clone 17a tra

291 ulture and prevents their degeneration after 6-hydroxydopamine treatment in vivo.

292 t was ablated by chemical sympathectomy with 6-hydroxydopamine treatment.

293 t was ablated by chemical sympathectomy with 6-hydroxydopamine treatment.

294 First, rats were exposed to a mild dose of 6-hydroxydopamine unilaterally into the nigrostriatal do

295 xperiment 1, rats received microinfusions of 6-hydroxydopamine unilaterally to induce dopamine termin

296 esion produced by intrastriatal injection of 6-hydroxydopamine was indistinguishable between WT and A

297 rplexiform cells (DA-IPCs) were destroyed by 6-hydroxydopamine was measured behaviorally.

298 In the present study, 6-hydroxydopamine was used to lesion the dorsal striatum

299 6-Hydroxydopamine was used to produce a model of Parkins

300 athway had been eliminated unilaterally with 6-hydroxydopamine, we injected a Cre-dependent virus cod